Ataxia talangiectasia mutated and Rad-3 related (ATR) kinase is an enzyme involved in the DNA damage response (DDR). This signaling network acts to detect and orchestrate a cell's response to certain forms of DNA damage, most notably double strand breaks and replication stress. Following treatment with many types of DNA damaging drugs and ionizing radiation, cells are reliant on the DDR for survival. It has been shown that disruption of the DDR can increase cancer cell sensitivity to these DNA damaging agents and thus may improve patient responses to such therapies. Inhibition of ATR is one approach that can be taken to disrupt the DDR and it has been shown that inhibition of ATR can markedly increase cancer cell sensitivity to DNA damaging agents. To support the clinical progression of ATR inhibitors it is necessary to develop biomarkers that can measure the degree of ATR inhibition or the impact ATR inhibition has on cellular DNA damage.